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  • Title: Speeding of oxygen uptake kinetics is not different following low-intensity blood-flow-restricted and high-intensity interval training.
    Author: Corvino RB, Oliveira MFM, Denadai BS, Rossiter HB, Caputo F.
    Journal: Exp Physiol; 2019 Dec; 104(12):1858-1867. PubMed ID: 31613029.
    Abstract:
    NEW FINDINGS: What is the central question of this study? Can interval blood-flow-restricted (BFR) cycling training, undertaken at a low intensity, promote a similar adaptation to oxygen uptake ( V̇O2 ) kinetics to high-intensity interval training? What is the main finding and its importance? Speeding of pulmonary V̇O2 on-kinetics in healthy young subjects was not different between low-intensity interval BFR training and traditional high-intensity interval training. Given that very low workloads are well tolerated during BFR cycle training and speed V̇O2 on-kinetics, this training method could be used when high mechanical loads are contraindicated. ABSTRACT: Low-intensity blood-flow-restricted (BFR) endurance training is effective to increase aerobic capacity. Whether it speeds pulmonary oxygen uptake ( V̇O2p ), CO2 output ( V̇CO2p ) and ventilatory ( V̇Ep ) kinetics has not been examined. We hypothesized that low-intensity BFR training would reduce the phase 2 time constant (τp ) of V̇O2p , V̇CO2p and V̇Ep by a similar magnitude to traditional high-intensity interval training (HIT). Low-intensity interval training with BFR served as a control. Twenty-four participants (25 ± 6 years old; maximal V̇O2 46 ± 6 ml kg-1  min-1 ) were assigned to one of the following: low-intensity BFR interval training (BFR; n = 8); low-intensity interval training without BFR (LOW; n = 7); or high-intensity interval training without BFR (HIT; n = 9). Training was 12 sessions of two sets of five to eight × 2 min cycling and 1 min resting intervals. LOW and BFR were conducted at 30% of peak incremental power (Ppeak ), and HIT was at ∼103% Ppeak . For BFR, cuffs were inflated on both thighs (140-200 mmHg) during exercise and deflated during rest intervals. Six moderate-intensity step transitions (30% Ppeak ) were averaged for analysis of pulmonary on-kinetics. Both BFR (pre- versus post-training τp  = 18.3 ± 3.2 versus 14.5 ± 3.4 s; effect size = 1.14) and HIT (τp  = 20.3 ± 4.0 versus 13.1 ± 2.9 s; effect size = 1.75) reduced the V̇O2p τp (P < 0.05). As expected, there was no change in LOW ( V̇O2p τp  = 17.9 ± 6.2 versus 17.7 ± 4.3 s; P = 0.9). The kinetics of V̇CO2p and V̇Ep were speeded only after HIT (38.5 ± 10.6%, P < 0.001 and 31.2 ± 24.7%, P = 0.004, respectively). Both HIT and low-intensity BFR training were effective in speeding moderate-intensity V̇O2p kinetics. These data support the findings of others that low-intensity cycling training with BFR increases muscle oxidative capacity.
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